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KDM3B suppresses APL Progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137105 | GEO | 2020/04/10

REPOSITORIES: GEO

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KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RAR?.

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KDM3B suppresses APL Progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα (ChIP-seq data set)

Project description:Histone demethylase KDM3B is considered to play a critical role in leukemogenesis. To the best of our knowledge, this study is the first attempt to probe the detailed genetic and epigenetic mechanisms underlying the regulation of KDM3B in the development of APL from the perspectives of multi-layer omics. Results of the present study demonstrate that KDM3B exerts anti-APL effect by directly modulating H3K9me1/me2 levels to maintain compact chromatin status, but also indicate the interaction between KDM3B and PML/RARα regulates degradation of PML/RARα.

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KDM3B suppresses APL Progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα

Project description:KDM3B suppresses APL Progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα

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KDM3B suppresses APL Progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARα (ChIP-seq data set)

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KDM5A suppresses PML-RARα target gene expression and APL differentiation through repressing H3K4me2

Project description:Epigenetic abnormalities are frequently involved in the initiation and progression of cancers including acute myeloid leukemia (AML). A subtype of AML, Acute promyelocytic leukemia (APL), is mainly driven by a specific oncogenic fusion event of PML-RARα. PML-RARα was reported as a transcription repressor through the interaction with NCoR/HDAC complexes leading to the mis-suppression of its target genes and differentiation blockage. While previous studies were mainly focused on the connection of histone acetylation, it is still largely unknown whether alternative epigenetics mechanisms are involved in APL progression. KDM5A is a demethylase of histone H3 lysine 4 di- and tri- methylations (H3K4me2/3) and a transcription corepressor. Here, we found that the loss of KDM5A led to APL NB4 cell differentiation and retarded growth. Mechanistically, through epigenomics and transcriptomics analyses, we detected KDM5A binding in 1,889 genes, with the majority of the binding events at promoter regions. KDM5A suppressed the expression of 621 genes, including 42 PML-RARα target genes primarily by controlling the H3K4me2 in the promoters and 5’ end intragenic regions. In addition, a recently reported pan-KDM5 inhibitor, CPI-455 on its own could phenocopy the differentiation effects as KDM5A loss in NB4 cells. CPI-455 treatment or KDM5A knockout could greatly sensitize NB4 cells to ATRA induced differentiation. Our findings indicated that KDM5A contributed to the differentiation blockage in the APL cell line NB4, and inhibition of KDM5A could greatly potentiate NB4 differentiation.

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Expression data from PML-RARα transgenic mouse APL(acute promyelocyte leukemia) cells

Project description:The differentiation of leukemia stem cells (LSCs) is generally regarded as a one-way alterative process to self-renewal. However, how differentiation impacts LSC stemness has largely been unexplored. Here we show that before reaching terminal differentiation (TD), apical LSCs of mouse acute promyelocytic leukemia passed through a partial differentiation (PD) stage, wherein the leukemia cells re-initiated leukemia via de-differentiation albeit at a reduced rate. Notably, while retinoic acid (RA) preferentially drove the transition of LSC to PD, monocytic Irf8 skewed PD cells to terminal maturation over de-differentiation and/or expansion. Remarkably, the combined use of RA and Irf8 induction depleted the total leukemogenic potential, which indicates that discrete stage- or lineage-specific mechanisms elaborate a step-wise LSC differentiation. We used microarrays to detail the global programme of gene expression indicating the molecular mechanisms unerlying the the process of LSC step-wise differentiation. Retroviral GFP-labled mouse APL cells (bone marrow sample) were repopulated in vivo through transplantation into syngenic recipients. At the proper time points, the GFP positive APL bone marrow cells were collected and sorted for UNSC, UNPD and UNTD samples through FACS. RA-PD and RA-TD cells were sorted from bone marrow tissue treated with ATRA (all trans retinoic acid) for 5 days. The freshly isolated samples were then lysed for RNA extration. Each sample had two biological replicates.

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Regulation of NF-κB by PML and PML-RARα.

Project description: Not available

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